Biology Reference
In-Depth Information
and European
Vipera
, with the high reactogenicity of the larger doses of antivenom
required to treat some snakebites (Cardoso et al., 1993) further illustrates this impor-
tant point (Chippaux and Boyer, 2010). The mechanism of the vast majority of anti-
venom reactions has nothing to do with acquired hypersensitivity or IgE, but to
complement activation by aggregates of IgG or its fragments, or to osmotic effects
of the large intravenously administered bolus of antiserum protein. In a prospective
review of 147 patients who presented with snakebites in a rural South African hospital,
13 out of 17 treated with SAVP/SAIMR polyvalent antivenom developed early, poten-
tially severe anaphylactic reactions (including urticaria, bronchospasm, angioedema,
and hypotension; Moran et al., 1998).
Current evidence contraindicates pretreatment with epinephrine, antihistamines, or
glucocorticoids (
Table 4.3
; Weinstein et al., 2009). However, a recent low-power study
compared the incidence of early reactions in envenomed patients given pretreatment
with i.v. hydrocortisone and diphenhydramine and in whom diluted antivenom was
infused over 1 h, to historical controls prior to slow infusion of equine-derived anti-
venom with those who had no premedication and in whom undiluted antivenom was
given via i.v. push injection over about 10 min (Caron et al., 2009). This investigation
suggested that premedication combined with slow administration of diluted antivenom
might reduce the frequency and severity of antivenom-related reactions. In reviewing
the literature, the authors found no convincing evidence that corticosteroid, histamine
(H-1) blockers, or epinephrine, used singly or in combination, significantly decreased
the incidence of antivenom reactions (Caron et al., 2009). Another study reported that
discretionary use of premedication did not reduce the frequency of reactions (Isbister et
al., 2009). Therefore, until further study clarifies this issue, antivenom is best adminis-
tered with slow i.v. infusion following a standard dilution (see
Table 4.3
). In the event
of a reaction (urticaria, wheeze/rhonchi, angioedema, laryngospasm, hypotension, GI
symptoms, etc.), the infusion should be discontinued and the patient should immedi-
ately be given i.m. epinephrine urgently, followed by an i.v. antihistamine H-1 blocker
such as chlorpheniramine, and i.v. hydrocortisone. Patients with severe bronchocon-
striction/spasm should be given nebulized salbutamol (or another β
2
-agonist) for rhon-
chus/wheeze. When the reaction has subsided, the antivenom infusion can be resumed
at a slower rate in order to complete the full dose, but with continued close vigilance
for any signs of further reaction. The risk of early anaphylactic reactions is one reason
why use of antivenom by nonmedically qualified persons outside of a medical facility
is discouraged. It emphasizes the need to provide antivenom in a hospital setting (e.g.,
Level I-II trauma facility) that is fully equipped to manage a patient with life-threaten-
ing anaphylaxis.
A Further Comment on Thelotornis Envenoming and the Lack of
Commercial Antivenom
As there is no anti-
Thelotornis
antivenom commercially available, it is fortunate that
envenoming from
Thelotornis
spp. is so rare. In any case of serious
Thelotornis
enven-
oming, consultation with an experienced clinical toxinologist via a poison control cen-
ter is mandatory. Treatment must therefore focus on managing hemostatic deficiencies
resulting from the consumptive coagulopathy and hemorrhagic diathesis. Although
